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PubMedDate not supplied

Effect of intravenous fat on cholecystokinin secretion and gallbladder motility in man.

During total parenteral nutrition (TPN) gallbladder bile stasis and hypomotility have been well documented. Little is known, however, about the effect of the separate components of TPN on gallbladder motor function. Inasmuch as fat, administered intraduodenally, is a potent stimulus of cholecystokinin (CCK) secretion and gallbladder contraction we have investigated whether intravenous (IV) fat affects gallbladder motility. Six healthy volunteers were studied on two separate occasions, during infusion of Intralipid 10%, 200 mL/h or saline infusion (control) for 3 hours, to evaluate the effect of IV infusion of fat on (1) plasma CCK concentration and gallbladder volume and (2) CCK-induced gallbladder emptying. Intravenous infusion of Intralipid resulted in significant increases in serum triglycerides from 0.9 +/- 0.1 to 5.1 +/- 1.3 mmol/L (at 90 min). During fat infusion no significant changes in plasma CCK and gallbladder volume were noted when compared with basal values or to the control experiment. During IV fat, concomitant infusion of 0.25, 0.5, and 1.0 Ivy dog unit (IDU) per kilogram per hour of CCK-33 resulted in a significant reduction in gallbladder volume from 26 +/- 6 cm3 (basal) to 15 +/- 4 cm3 (p less than .05), 6 +/- 2 cm3 (p less than .05) and 2.5 +/- 1 cm3 (p less than .05), respectively. No significant differences in CCK-induced gallbladder emptying were observed between IV fat and saline infusion (control). It is concluded that, in contrast to intraduodenal fat, IV infusion of fat does not affect (1) basal plasma CCK and gallbladder volume and (2) CCK-induced gallbladder contraction.

Adult↗
PubMed1993

Gallbladder dynamics in chronic pancreatitis. Relationship to exocrine pancreatic function, CCK, and PP release.

Gallbladder dynamics, cholecystokinin (CCK), and pancreatic polypeptide (PP) release were studied in 14 patients with chronic pancreatitis (CP) (2 females, 12 males; age range 24-56 years) and 12 control subjects (4 females, 8 males, 21-50 years). On day 1, gallbladder contractility was investigated after ceruletide intravenous infusion (2.5 ng/kg/min for 10 min). On day 2, a mixed standard test meal (1450 kJ) was administered orally. Gallbladder volume was assessed at three time intervals before (-30, -15, 0 min) and at 5, 10, 20, 30, 40, 50, 60, 80, 100 and 120 min after stimulation by means of ultrasonography. CCK and PP plasma levels were determined at each time interval. Exocrine pancreatic function was assessed using the pancreolauryl serum test (PLT). Six patients with CP had severe exocrine pancreatic insufficiency (EPI) (PLT < 1.8 micrograms/ml) with steatorrhea, eight patients had mild-moderate EPI. Fasting gallbladder volume was increased in CP (32.3 +/- 3.1 cm3) as compared to controls (20.5 +/- 1.2 cm3) (P < 0.01). Peak gallbladder contraction (percent of initial volume) in CP ranged from 5 to 55% (controls: 8-46%) following ceruletide and from 17 to 86% (controls: 27-80%) following the test meal (NS). There was no correlation between the degree of EPI according to PLT and peak gallbladder contraction. Gallbladder emptying in CP patients was not different from controls, although the postprandial CCK response was significantly impaired (P < 0.01). Postprandial PP response in CP was correlated with the PLT result (r = 0.78; P < 0.01) but not with gallbladder emptying or refilling time.(ABSTRACT TRUNCATED AT 250 WORDS)

Adult↗
PubMed2003

Risk factors for symptomatic gallstones in patients with liver cirrhosis: a case-control study.

OBJECTIVES: Liver cirrhosis is a well-documented risk factor for the formation of gallstones. In cirrhotic patients, gallstones are almost always "silent," and surgery is rarely required. When indicated (symptoms or complications), cholecystectomy implies a high morbidity risk in these patients, especially in the advanced stages of cirrhosis. The aim of this study was to estimate the risk factors for symptom development in cirrhotic patients with gallstones to identify the subgroup of patients at risk of undergoing surgery. METHODS: A total of 140 patients with liver cirrhosis and gallstones were studied: 97 with asymptomatic and 43 with symptomatic gallstone disease. The risk factors for gallstone formation (age, gender, family history, parity, obesity, diabetes mellitus, hyperlipoproteinemia) and the characteristics of liver cirrhosis (etiology, duration, Child class, hypersplenism), gallstones (duration, number, size), and gallbladder (size, wall thickness) were assessed in all patients. In 12 patients (four symptomatic, eight asymptomatic), gallbladder emptying was also evaluated by ultrasound. The association of asymptomatic and symptomatic gallstones with all these parameters was statistically evaluated by Student's t, Mann-Whitney, and chi(2) tests, as well as by means of multiple logistic regression. The causal relationship between these characteristics and gallstone symptoms was also examined by means of the KDD (knowledge discovery from databases) method, with an algorithm for learning Bayesian networks. RESULTS: Advanced age, female gender, viral etiology of cirrhosis, family history of gallstones, and duration of gallstone disease were significantly associated with symptomatic gallstone disease. The number or size of gallstones and the size or emptying of the gallbladder did not differ in symptomatic versus asymptomatic patients. Male gender and alcoholic cirrhosis were inversely correlated with symptom presence. In the multivariate analysis, family history (p = 0.0098) and advanced age (p = 0.0422) were positively correlated and male gender (p = 0.0049) and alcoholic etiology of cirrhosis (p = 0.0116) negatively correlated with symptom presence. These relationships (except for age) were also evidenced by the KDD method. CONCLUSIONS: The risk of gallstones becoming symptomatic is significantly lower in men and in alcoholic cirrhosis. In cirrhotic women, and especially in the presence of a positive family history and of advanced age, the risk of developing symptoms and undergoing surgery was significantly greater.

Adult↗
PubMed1995

Gender influences sphincter of Oddi response to cholecystokinin in the prairie dog.

Although gallstones and disorders of biliary tract motility are both more common in women than men, sphincter of Oddi motility has not previously been compared between the sexes. In this study, cholescintigraphy (under ketamine and diazepam anesthesia) was used to determine gallbladder emptying rate and ejection fraction in response to cholecystokinin (CCK) in eight male and six female prairie dogs fed a nonlithogenic diet. Ten days later, under alpha-chloralose anesthesia, sphincter of Oddi phasic wave activity was monitored for 10-min intervals before (control), during 20 min of CCK infusion, and for 20 min after infusion. Gallbladder emptying rate and ejection fraction and baseline sphincter of Oddi frequency, amplitude, and motility index (= frequency x amplitude) did not differ significantly between the sexes. Sphincter of Oddi phasic wave frequency was increased during CCK infusion in both males and females, but the change in amplitude was significantly greater in females, than males. We conclude that the increased incidence of biliary tract disease in women may be due to altered sphincter of Oddi hormonal response.

Animals↗
PubMed1993

Effect of extracorporeal shock wave lithotripsy and ursodeoxycholic acid on gallbladder motility.

Extracorporeal shock wave lithotripsy and dissolution agents are useful nonsurgical therapies for gallstones. Their effect on gallbladder emptying is unclear. We evaluated emptying by ultrasonography before and after lithotripsy in 50 patients on ursodeoxycholic acid or placebo and in nine controls. At baseline, patients had normal (68.8 +/- 3.2%) or delayed emptying (14.5 +/- 3.3%). In a subset of 24 patients, lithotripsy increased fasting volume (26.6 +/- 3.0 to 43.8 +/- 5.0 ml, P < 0.005), postprandial volume (11.3 +/- 3.1 ml to 22.9 +/- 3.0 ml, P < 0.05), and decreased ejection fraction (70.0 +/- 4.1% to 42.7 +/- 6.0%, P < 0.0005). There was an inverse linear correlation between power and ejection fraction, r = -0.43, P < 0.005. Ursodeoxycholic acid increased fasting (23.3 +/- 2.2 ml to 36.7 +/- 4.6 ml, P < 0.005) and postprandial volume (11.1 +/- 1.8 to 17.6 +/- 2.5, P < 0.005). Treatment with ursodeoxycholic acid resulted in a greater decrease in fragment size compared to placebo after lithotripsy in patients with fragment size greater than 6 mm. In conclusion, both lithotripsy and ursodeoxycholic acid have an effect on gallbladder emptying.

Adult↗
PubMed1998

Endogenous cholecystokinin enhances postprandial gastroesophageal reflux in humans through extrasphincteric receptors.

BACKGROUND & AIMS: Exogenous cholecystokinin (CCK) decreases lower esophageal sphincter (LES) pressure and increases transient LES relaxations (TLESRs) in humans. The aims of this study were to determine whether endogenous CCK increases gastroesophageal reflux in humans and whether this is a direct effect on the LES. METHODS: Esophageal pH, LES pressure, and gallbladder volume were measured in 8 healthy volunteers after ingestion of a 181-kcal meal alone or adding 12 g cholestyramine to increase endogenous CCK release. In 7 additional volunteers, the effect of cholestyramine was studied during intravenous perfusion of saline or the CCK-A receptor antagonist loxiglumide. In circular LES strips from 9 transplant donors, we measured the effect of CCK-8 (10(-11) to 3 x 10(-8) mol/L) on basal tension and on electrical field-induced relaxation. RESULTS: Cholestyramine increased gallbladder emptying, reflux episodes, TLESRs, and time of esophageal pH of <4. Loxiglumide inhibited postprandial gallbladder emptying, reflux episodes, TLESRs, and time of pH of <4 and prevented the decrease in LES pressure induced by cholestyramine. In vitro, CCK-8 contracted LES strips through a tetrodotoxin-insensitive pathway but did not modify electrical field-induced LES relaxations. CONCLUSIONS: Endogenous CCK enhances postprandial gastroesophageal reflux in humans by increasing the rate of TLESRs and reduces postprandial LES pressure. These actions seem mediated by extrasphincteric CCK-A receptors that override a direct contractile effect of CCK on the LES muscle.

Adult↗
PubMed2003

Differential effects of motilin on interdigestive motility of the human gastric antrum, pylorus, small intestine and gallbladder.

Motilin was infused in this study with the aim of examining refractory characteristics for motilin stimulation of antral phase III and fasting gallbladder emptying. Moreover, interdigestive pyloric and small intestinal motility from duodenum to ileum were studied, as these may be target organs for motilin. Eight fasting, healthy male volunteers received, on separate subsequent days, repeated infusions of 13leucine-motilin (8 pmol (kg min)(-1) for 5 min) or saline at 30 min after phase IIIs in the duodenum. Interdigestive motility of the antrum, pylorus, duodenum, jejunum and ileum was measured for maximum 10 h by using a 21-lumen perfused catheter. Gallbladder motility was measured by ultrasonography. Motilin infusions induced antral phase IIIs, but only after a preceding phase III of duodenal origin. Under this condition, time-interval to phase III at the duodenal recording site was 30 +/- 13 (SEM) min after motilin, compared with 79 +/- 14 min after saline (P < 0.01), and compared with 121 +/- 13 min for motilin infusion following an antral phase III (P < 0.001). Motilin did not affect small intestinal motility or isolated pyloric pressure waves (IPPWs). However, the number of IPPWs was significantly affected by the origin of the preceding phase III, irrespective of whether motilin or saline was infused. Gallbladder volume decreased significantly within 10 min after each motilin infusion. We conclude that this study clearly demonstrates differential regional effects of motilin. Motilin initiates antral phase IIIs, but stimulation is subject to a refractory period which is clearly prolonged after a preceding antral phase III. Motilin induced gallbladder emptying, however, is not subject to a refractory state. Small intestinal phase IIIs as well as pyloric IPPWs are not affected by motilin.

Adult↗
PubMed1998

Plasma cholecystokinin and gallbladder responses to increasing doses of bombesin in celiac disease.

Impaired postprandial gallbladder emptying in celiac disease has been attributed to an absence of appropriate cholecystokinin release. To determine if a flat jejunal mucosa in celiac patients is related to a reduced cholecystokinin-secreting capacity, increasing doses of bombesin were infused into six patients with celiac disease and a flat jejunal mucosa (group A), in seven celiac patients with a normal jejunal mucosa while on a gluten-free diet (group B), and in seven healthy controls (group C). Bombesin induced significant (P < 0.05) increments of plasma CCK to a maximum value of 1.0 +/- 0.3 pM in group A, to 1.5 +/- 0.3 pM in group B, and to 1.2 +/- 0.3 pM in group C (NS between groups), that were accompanied by significant (P < 0.05) gallbladder emptying responses of 70 +/- 4% in group A, 47 +/- 10% in group B and 65 +/- 5% in group C. Dose-response relationships were not different between groups. We conclude that there is no major impairment of gallbladder responsiveness to bombesin or of cholecystokinin-secreting capacity in patients with a flat jejunal mucosa due to celiac disease.

Adult↗
PubMed1984

Gallbladder dynamics induced by a fatty meal in normal subjects and patients with gallstones: concise communication.

A study was undertaken to establish the pattern of gallbladder emptying in normal subjects and in patients with gallstones, using a fatty meal as stimulus to release endogenous cholecystokinin. The time from meal ingestion to beginning of gallbladder emptying (latent period), the total duration of emptying (ejection period), degree of emptying (ejection fraction), and the rate of emptying (ejection fraction/ejection period) were measured noninvasively by a nongeometric scintigraphic technique. The mean latent period and ejection rate were similar in normal subjects and patients with gallstones, but the mean ejection period and ejection fraction were significantly reduced in the patients. This study suggests that for an identical stimulus, the gallbladder in cholelithiasis begins to empty at the normal time but empties for a shorter duration; the result is a reduction of ejection fraction but not of ejection rate.

Adult↗
PubMed1989

Delayed plasma cholecystokinin and gallbladder responses to intestinal fat in patients with Billroth I and II gastrectomy.

This study was undertaken to examine the intestinal phase of cholecystokinin (CCK) secretion and gallbladder contraction in patients who had undergone partial gastrectomy. Plasma CCK concentrations, measured by radioimmunoassay, and gallbladder contraction, measured by cholescintigraphy, were studied after intestinal administration of fat. Fasting plasma CCK concentrations were in the same range in nine patients who had undergone Billroth I gastrectomy (1.0 +/- 0.2 pmol/L), in nine patients who had undergone Billroth II gastrectomy (1.4 +/- 0.2 pmol/L), and in nine normal subjects (1.5 +/- 0.4 pmol/L). The peak increments in plasma CCK after intestinal fat were significantly (p less than 0.05) lower in patients with partial gastrectomy (5.4 +/- 0.6 pmol/L) compared with normal subjects (7.9 +/- 0.8 pmol/L). The integrated plasma CCK secretion was significantly (p less than 0.01 to p less than 0.05) reduced during the first 30 minutes in patients after Billroth I (74 +/- 11 pmol/1.30 min) and Billroth II gastrectomy (51 +/- 11 pmol/1.30 min) compared with normal subjects (122 +/- 18 pmol/1.30 min). Similarly, the start of gallbladder emptying was significantly (p less than 0.05) delayed in patients after partial gastrectomy. After 1 hour, however, the integrated plasma CCK response and gallbladder emptying were in the same range in Billroth I patients (186 +/- 34 pmol/1.60 min, 60% +/- 7%), Billroth II patients (175 +/- 17 pmol/1.60 min, 63% +/- 7%) and normal subjects (190 +/- 18 pmol/1.60 min, 55% +/- 6%). It is concluded that in patients who have undergone partial gastrectomy plasma CCK and gallbladder responses to intestinal fat are significantly delayed but reach normal levels beyond 30 minutes.

Adult↗
PubMed2002

[Effect of cholesterol in bile on cholecystokinin receptor in the gallbladder].

OBJECTIVE: To assess the effect of cholesterol in bile on cholecystokinin receptor (CCK-R) in the gallbladder. METHODS: One hundred Guinea pigs were randomly divided into four groups, 25 animals for each. The control group was fed a standard diet, and the cholesterol group fed a diet containing 2% cholesterol. After taking the 2% cholesterol diet for two weeks, the natural group persisted on the standard diet, and the treated group was perfused by traditional Chinese medicine. Serum cholecystokinin (CCK) level in the portal vein and maximal binding capacity (B(max)) and Kd of CCK-R in the gallbladder were measured in the four groups by RIA and RBA, and the concentrations of cholesterol in bile were also observed. RESULTS: Compared with the control group, after high-cholesterol feeding for two weeks, the gallbladder emptying rate [(65.83 +/- 7.32)% approximately (47.22 +/- 5.24)%] and B(max) of CCK-R [(60 +/- 27) approximately (32 +/- 13) fmol/mg protein] and in decreased fasting gallbladder volume (FV) [(0.89 +/- 0.26) approximately (1.34 +/- 0.61) cm(3)] and concentration of cholesterol [(0.44 +/- 0.11) approximately (0.60 +/- 0.13) mmol/L] in bile increased, but no change was in the serum CCK level and Kd of CCK-R in the cholesterol group. Compared with the natural group, after two-week in take of herb decoction of qingre lidan and liqi huoxue, FV [(1.27 +/- 0.60) approximately (0.90 +/- 0.27) cm(3)], RV [(0.85 +/- 0.45) approximately (0.32 +/- 0.12) cm(3)], FB [(0.92 +/- 0.35) approximately (0.73 +/- 0.21) cm(3)], RB [(0.76 +/- 0.34) approximately (0.29 +/- 0.08) cm(3)] in the treated group decreased significantly; but gallbladder emptying rate [(43.06 +/- 4.27)% approximately (67.01 +/- 6.82)%] increased significantly. The concentration of cholesterol in bile was lower in the treated group than in the natural group [(0.59 +/- 0.14) approximately (0.43 +/- 0.10) mmol/L], but no change was found in the serum CCK level. Bmax of CCK-R in the treated group increased significantly [(39 +/- 19) approximately (59 +/- 11) fmol/mg protein], Kd of CCK-R showed no significant changes between the treated group and natural group. CONCLUSION: High cholesterol in gallbladder bile causes defective muscle contraction by down-regulating CCK-R in the gallbladder, so the reduction of cholesterol concentration of bile may contribute to gallbladder contraction.

Animals↗
PubMed1995

Effect of aspirin on gallbladder motility in patients with gallstone disease. A randomized, double-blind, placebo-controlled trial of two dosage schedules.

Patients with gallstone disease have impaired gallbladder motility. Prostaglandins are thought to be important mediators of gallbladder hypomotility. We assessed the effect of aspirin, a prostaglandin inhibitor on gallbladder resting volume and ejection fraction according to a double-blind study protocol in 20 healthy volunteers and 30 patients with gallstone disease. Healthy volunteers had a higher ejection fraction compared to patients with gallstone disease (73.9 +/- 0.9% vs 60.4 +/- 1.0%, P < 0.05). Aspirin in a dose of 350 mg/day for two weeks did not alter gallbladder motility in the healthy volunteers. Thirty patients with gallstone disease were randomized into three treatment groups: group I (placebo), group II (aspirin 350 mg/day), and group III (aspirin 1400 mg/day). After two weeks of treatment, gallbladder ejection fraction was improved in group II (74.0 +/- 1.7% vs 62.0 +/- 1.7%, P < 0.01) and group III (69.8 +/- 3.8% vs 61.2 +/- 1.3%, P < 0.01) but not in group I (60.4 +/- 2.6% vs 59.0 +/- 1.9%, P = NS). The higher dose of aspirin did not induce a greater increase in gallbladder emptying. It is concluded that impaired gallbladder motility in patients with gallstone disease is corrected by short-term oral aspirin even in low dosage. This may be clinically useful in secondary prophylaxis after nonsurgical therapy for gallstone disease.

Adult↗
PubMed2001

Gallbladder muscle dysfunction in patients with chronic acalculous disease.

BACKGROUND & AIMS: The mechanisms responsible for the abnormalities of gallbladder emptying in patients with chronic acalculous gallbladder disease (AGD) have not been elucidated. This study was designed to determine whether a muscle defect could explain this gallbladder dysfunction. METHODS: Gallbladder contraction induced by a continuous intravenous cholecystokinin octapeptide (CCK-8) infusion was determined by ultrasonography in control subjects, patients with AGD, pigment stones, and cholesterol stones. Muscle cells were obtained by enzymatic digestion. (125)I-CCK-8 binding and [(35)S]guanosine triphosphate gamma S (GTP gamma S) binding studies were performed. RESULTS: In vivo gallbladder contraction induced by CCK-8 was significantly lower in AGD (29.4%) and cholesterol stones (28.8%) than in pigment stones (59.8%) and normal controls (57.8%; P < 0.01). In vitro muscle cell contraction induced by CCK-8 was also lower in AGD than in pigment stones. It remained impaired in AGD after stimulation with the G-protein activators GTP gamma S and AlF(4) and with the second messenger 1,2-dioctanoyl-sn-glycerol. However, GTP gamma S binding induced by CCK-8 and vasoactive intestinal polypeptide and the binding capacity of CCK receptors were not different between AGD and pigment stones. CONCLUSIONS: These findings suggest that there is a good correlation between in vivo and in vitro gallbladder response to CCK-8 in patients with AGD. Unlike those found in cholesterol stones, the muscle defects in AGD appear to reside in the contractile apparatus.

Cell Membrane↗
PubMed1997

Inhibitory effect of bile salts on gallbladder smooth muscle contractility in the guinea pig in vitro.

BACKGROUND & AIMS: Impaired gallbladder emptying occurs in patients undergoing bile salt therapy for cholesterol gallstone dissolution and in patients with cirrhosis who have elevated serum bile salt concentrations. To determine if bile salts directly inhibit gallbladder contractility, isometric contraction of the guinea pig gallbladder was examined in vitro. METHODS: Contractile responses to cholecystokinin (CCK), bethanechol, KCI, and field stimulation were constructed alone and in the presence of selected bile salts: taurodeoxycholate (TDC), taurochenodeoxycholate, taurocholate, and tauroursodeoxycholate (TUDC). RESULTS: More hydrophobic bile salts, such as TDC (as low as 5 micromol/L), concentration-dependently depressed (P < 0.05) both CCK- and field stimulation-induced gallbladder contractions. More hydrophilic bile salts, such as TUDC, only caused a modest depression up to a concentration of 500 micromol/L. When 5 or 50 micromol/L of TUDC was added to the organ bath before the application of equalmolar TDC, the TDC-induced impaired gallbladder contractility was reversed. Thus, this inhibitory effect on gallbladder contraction depended on the hydrophobicity of bile salts and was also specific for certain stimuli such as CCK and field stimulation (mediated by cholinergic nerves, being abolished by atropine and tetrodotoxin). CONCLUSIONS: Such direct bile salt inhibition of CCK- and cholinergic nerve-induced gallbladder contraction may contribute to the deteriorating gallbladder emptying in patients undergoing bile salt therapy for stone dissolution and in cirrhotic patients who are at risk for gallstone formation.

Animals↗
PubMed2002

Evaluation of gastrointestinal solubilization of petroleum hydrocarbon residues in soil using an in vitro physiologically based model.

Petroleum hydrocarbon residues in weathered soils may pose risks to humans through the ingestion pathway. To understand the factors controlling their gastrointestinal (GI) absorption, a newly developed experimental extraction protocol was used to model the GI solubility of total petroleum hydrocarbon (TPH) residues in highly weathered soils from different sites. The GI solubility of TPH residues was significantly higher for soil contaminated with diesel than with crude oil. Compared to the solubility of TPH residues during fasted state,the solubility of TPH residues during fat digestion was much greater. Diesel solubility increased from an average of 8% during the "gallbladder empty" phase of fasting (and less than 0.2% during the otherfasting phase) to an average of 16% during fat digestion. For crude oil, the solubility increased from an average of 1.2% during the gallbladder empty phase of fasting (and undetectable during the other fasting phase) to an average of 4.5% during fat digestion. Increasing the concentration of bile salts also increased GI solubility. GI solubility was reduced by soil organic carbon but enhanced by the TPH content.

Absorption↗
PubMed1997

Cholestyramine influences meal-stimulated pancreaticobiliary function and plasma cholecystokinin independent of gastric emptying and food digestion.

BACKGROUND: Cholestyramine enhances gallbladder emptying and plasma cholecystokinin responses to oral ingestion of a mixed meal. It is not known whether this effect occurs independently of alterations in gastric emptying or maldigestion of nutrients. METHODS: We perfused 15 g of an amino acid meal intraduodenally for 60 min in seven healthy volunteers, once with and once without cholestyramine. Intraduodenal perfusion of saline with or without cholestyramine (6 g/h) was started 60 min before the amino acid meal and continued for 2 h. RESULTS: Cholestyramine markedly enhanced the incremental plasma cholecystokinin response to the meal from 36 +/- 12 to 139 +/- 25 pmol/l x 60 min (P < 0.005), incremental amylase output from 2.4 +/- 0.7 to 5.7 +/- 0.7 kU/h (P < 0.05), and incremental integrated gallbladder contraction from 1948 +/- 235 to 2840 +/- 189% x 60 min (P < 0.05). CONCLUSION: The enhancing effect of cholestyramine on postprandial gallbladder contraction, pancreatic enzyme secretion, and plasma cholecystokinin release is not dependent on gastric emptying rates or appropriate digestion of nutrients.

Adult↗
PubMed1988

Gallbladder function during gallstone dissolution. Effect of bile acid therapy in patients with gallstones.

Impaired gallbladder emptying has been associated with gallstone disease but any effect on or from bile acid therapy for gallstone dissolution is unknown. We evaluated gallbladder filling and emptying with low-dose cholecystokinin infusion (0.02 U/kg.h) by computer-assisted cholescintigraphy in 52 controls versus 31 gallstone patients: 17 treated with 12-15 mg/kg.day of chenodeoxycholic acid and 14 with 8-10 mg/kg.day of ursodeoxycholic acid. Thirteen of 31 patients with complete dissolution had four scans: before, after 3 mo of therapy, after stone dissolution, and after discontinuation of bile acids. The 18 failures had three scans: before and after 3 and 15-18 mo of therapy. Before therapy, the 31 gallstone patients had significantly impaired gallbladder emptying compared with controls, but filling was not decreased. Bile acids significantly decreased emptying in both treatment groups after 3 mo of therapy. In the dissolution group, emptying improved once the stones had dissolved and increased further upon discontinuing the bile acids. In the failures, impaired emptying persisted for up to 15-18 mo. Gallbladder filling in the 31 gallstone patients was also significantly decreased after 3 mo of bile acid therapy, particularly in the failure patients, 5 of whom exhibited zero filling. No differences were detected between ursodeoxycholic acid and chenodeoxycholic acid for either gallbladder function or efficiency of dissolution. Thus, bile acid therapy impairs gallbladder filling and emptying in gallstone patients. Gallstone dissolution improves emptying, which is further enhanced when bile acids are discontinued.

Adult↗
PubMed1991

Gallbladder sensitivity to cholecystokinin in coeliac disease. Correlation of gallbladder contraction with plasma cholecystokinin-like immunoreactivity during infusion of cerulein.

The present study was undertaken to determine whether alterations in the gallbladder sensitivity to cholecystokinin (CCK), apart from a reduced endogenous CCK secretion, contribute to the abnormally decreased postprandial gallbladder contraction in patients with coeliac disease. Gallbladder emptying, measured by cholescintigraphy, and plasma CCK levels, measured by radioimmunoassay, were studied during infusion of graded doses of the CCK analog cerulein in six coeliac patients with subtotal villous atrophy, six coeliac patients on a gluten-free diet with normal villous architecture, and nine control subjects. Both in the patients and in the controls infusion of stepwise increasing doses of cerulein, in the range of 1-16 ng.kg-1.h-1, induced dose-related changes in plasma CCK-like immunoreactivity (CCK-LI) (r = 0.99; p less than 0.001) and gallbladder emptying (r greater than 0.97; p less than 0.01-p less than 0.001). Plasma CCK-LI and gallbladder responses were not significantly different among untreated coeliac patients, treated coeliac patients, and controls. Gallbladder sensitivity to cerulein in untreated and treated coeliac patients was not significantly different from that in controls. It is concluded that the abnormally decreased gallbladder contraction in coeliac patients is the result of a reduced endogenous CCK secretion and not of a lack of end-organ responsiveness to CCK.

Celiac Disease↗